Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction
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RESEARCH ARTICLE
Biological Research Open Access
Altered thalamic neurotransmitters metabolism and functional connectivity during the development of chronic constriction injury induced neuropathic pain Zhifu Wang1, Sheng Huang2,3, Xiangmei Yu1, Long Li2,3, Minguang Yang2,3, Shengxiang Liang2,3, Weilin Liu4 and Jing Tao4*
Abstract Background: To investigate the thalamic neurotransmitters and functional connections in the development of chronic constriction injury (CCI)-induced neuropathic pain. Methods: The paw withdrawal threshold was measured by mechanical stimulation the right hind paw with the von frey hair in the rats of CCI-induced neuropathic pain. The N-acetylaspartate (NAA) and Glutamate (Glu) in thalamus were detected by magnetic resonance spectrum (MRS) process. The thalamic functional connectivity with other brain regions was scanned by functional magnetic resonance image (fMRI). Results: The paw withdrawal threshold of the ipsilateral side showed a noticeable decline during the pathological process. Increased concentrations of Glu and decreased levels of NAA in the thalamus were significantly correlated with mechanical allodynia in the neuropathic pain states. The thalamic regional homogeneity (ReHo) decreased during the process of neuropathic pain. The functional connectivity among the thalamus with the insula and somatosensory cortex were significantly increased at different time points (7, 14, 21 days) after CCI surgery. Conclusion: Our study suggests that dynamic changes in thalamic NAA and Glu levels contribute to the thalamic functional connection hyper-excitation during CCI-induced neuropathic pain. Enhanced thalamus-insula functional connection might have a significant effect on the occurrence of neuropathic pain. Keywords: Chronic pain, N-acetylaspartate (NAA), Glutamate (Glu), Central sensitization, Thalamic functional connectivity Introduction Neuropathic pain due to injuries or lesions in the peripheral nervous system is always accompanied by allodynia, hyperalgesia, and even numbness [1, 2]. The thalamus, which is the significant area activated as a response to
*Correspondence: [email protected] 4 College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China Full list of author information is available at the end of the article
noxious stimulation in normal subjects, has remained the focus of attention in the field of pain research in the past century [3]. Indeed, the thalamus becomes sensitized after a pain attack, reducing the hyperalgesia and allodynia threshold. Clinical studies have shown increased neural activity when patients encounter peripheral nerve injury [4, 5]. The reduction in the thalamic neural response threshold has also been investigated in rodent models [6, 7].
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